Left ventricular assist device (LVAD) thrombosis is a devastating complication that occurs in about 10% of patients despite anticoagulation and antiplatelet treatment. How the thrombus initiates and propagates is unknown. We pathologically and immunohistochemically examined 28 thrombi removed from 17 HeartMate II LVADs. Two groups of thrombi were found: those formed in the inlet/outlet and those on the rotor. The four thrombi found at the inlet (three inlet conduit and one inlet tube) and outlet (three at outlet elbow and one outlet graft) appeared similar and were composed of a loose meshwork of fibrin(ogen), von Willebrand factor, leukocytes, and aggregated platelets. The majority of the thrombi (20/28), however, were located on the rotor: nine at the inlet bearing, five on the rotor vanes, and six at the outlet bearing. Laminated thrombi formed around the inlet bearing in rings, an area of blood recirculation. The inner rings of the thrombus had fibrin and von Willebrand factor. Aggregated platelets were found in the outer thrombi rings, but limited evidence of platelets within the laminated thrombi was noted. The presence of distinct rings suggests development of the clot over time. The increased platelets in the outer rings of the inlet bearing thrombi would support further investigation into their role in thrombus growth. Initiating events require further investigation, but the fibrin-rich structure of HeartMate II thrombi suggests that alternative anticoagulation strategies are needed to prevent thrombosis in our LVAD patients.
From the *BloodCenter of Wisconsin, Milwaukee, Wisconsin
†Medical College of Wisconsin, Milwaukee, Wisconsin
‡University of Louisville, Louisville, Kentucky
§St Jude Medical, St. Paul, Minnesota.
Submitted for consideration September 2017; accepted for publication in revised form October 2017.
K. Sundareswaran is an employee of St. Jude Medical. A.E. Mast receives grant support from Novo Nordisk and received an honorarium from Siemens.
Funding for the study was provided by the Research and Education Program Fund, a component of the Advancing a Healthier Wisconsin endowment at the Medical College of Wisconsin, and by grant 8UL1TR000055 from the Clinical and Translational Science Award (CTSA) program of the National Center for Research Resources and the National Center for Advancing Translational Sciences. A.E. Mast is supported by NHLBI grant HL068835.
Correspondence: Lisa M. Baumann Kreuziger, BloodCenter of Wisconsin, 8733 Watertown Plank Road, Milwaukee, WI 53226. Email: Lisa.email@example.com.